High impact information on Slco2a1

• Inhibitors of other channels, such as the purinergic receptor P2X7 and the prostaglandin transporter PGT, had no effect on PGE2 release [1].
• Melatonin suppresses NO-induced apoptosis via induction of Bcl-2 expression in PGT-beta immortalized pineal cells [2].
• In the present study, we investigated whether melatonin would prevent nitric oxide (NO)-induced apoptotic death of PGT-beta immortalized pineal cells [2].
• To identify the cis-acting region responsible for pineal-specific expression of the TPH gene, we investigated a 6.1-kb 5'-flanking region of the mouse TPH gene using an immortalized pineal cell line (PGT-beta) derived from transgenic mice [3].
• To develop PGT-specific inhibitors with high affinity, we designed a library of triazine compounds and screened 1842 small molecules by using Madin-Darby canine kidney cells stably expressing rat PGT [4].

Biological context of Slco2a1

• The phosphorylation of PGT was proportional to the level of phosphorylation of p56lck [5].
• Through morphological and biochemical analyses, it was demonstrated that cell death induced by serotonin in PGT-beta cells shows classic apoptotic features [6].

Anatomical context of Slco2a1

• Pharmacological characterization of adenosine receptors in PGT-beta mouse pineal gland tumour cells [7].
• Immunohistochemical staining for 15-hydroxyprostaglandin dehydrogenase was relatively intense over airway smooth muscle, as was staining for the prostaglandin transporter over both airway smooth muscle and epithelium [8].

Associations of Slco2a1 with chemical compounds

• Tyrosine kinase activity was measured by using an exogenous substrate: polyamino acid glutamic acid-tyrosine (4:1) (PGT) [5].

Analytical, diagnostic and therapeutic context of Slco2a1

• 2. Expression of the two adenosine receptor subtypes A2B and A3 was detected in mouse pineal glands and PGT-beta cells by polymerase chain reaction and nucleotide sequencing [7].

References